CHAPTER 36 Potassium, Calcium, and Phosphate Homeostasis 667 • Fig. 36.21 Overview of the major hormones regulating plasma [Ca++]. Dashed lines indicate negative feedback. FGF-23, fibroblast growth factor 23; PTH, parathyroid hormone. (From Koeppen BM, Stanton BA. Renal Physiology. 5th ed. Philadelphia: Elsevier; 2013.)
Integrative Review of Parathyroid Hormone and Calcitriol on Ca++ and Pi Homeostasis
Fig. 36.21 , PTH has numerous effects on Ca++ and Pi homeostasis. Hypocalcemia is the major stimulus of PTH secretion. PTH stimulates bone resorption, increases urinary Pi excretion, decreases urinary Ca++ excretion, and stimulates production of calcitriol, which stimulates Ca++ and Pi absorption by the intestine. Because changes in Pi handling in bone, intestines, and kidneys tend to balance out, PTH increases plasma [Ca++] while having little effect on plasma [Pi]. Overall a rise in plasma PTH levels in response to hypocalcemia returns plasma [Ca++] to the normal range. A decline in plasma [Ca++] has the opposite effect.
Calcitriol (the active form of vitamin D) also plays an important role in Ca++ and Pi homeostasis (
Fig. 36.22
The primary action of calcitriol is to stimulate Ca++ and Pi absorption by the intestine. To a lesser degree it acts with PTH to release Ca++ and Pi from bone and to decrease Ca++ excretion by the kidneys. The net effect of calcitriol is to increase plasma [Ca++] and [Pi]. Thus the major stimuli of calcitriol production are hypocalcemia via PTH and hypophosphatemia (i.e., a low plasma [Pi]).
In the absence of glucocorticoids (e.g., in Addison’s disease), excretion of Pi is depressed, as is the ability of the kidneys to excrete titratable acid and to generate new HCO3 − . Growth hormone increases reabsorption of Pi by the proximal tubule. As a result, growing children are in positive Pi balance and have a higher plasma [Pi] than adults, and this elevated [Pi] is important for bone formation.
• Fig. 36.22 Activation of calcitriol (vitamin D3) and its effect on Ca++ and Pi homeostasis. Hypocalcemia (via PTH) and hypophosphatemia are the major stimuli of the metabolism of calcifediol to calcitriol in the kidneys. The net effect of calcitriol is to increase plasma [Ca++] and [Pi]. (From Koeppen BM, Stanton BA. Renal Physiology. 5th ed. Philadelphia: Elsevier; 2013.) 1.
K+ homeostasis is maintained by the kidneys, which adjust K+ excretion to match dietary K+ intake, and by the hormones insulin, epinephrine, and aldosterone, which regulate the distribution of K+ between the ICF and ECF compartments. Other events, such as cell lysis, exercise, and changes in acid-base balance and plasma osmolality, disturb K+ homeostasis and plasma [K+].
2.
Excretion of K+ by the kidneys is determined by the rate and direction of K+ transport by the distal tubule and collecting duct. Secretion of K+ by these tubular segments is regulated by plasma [K+], aldosterone, and AVP. In contrast, changes in tubular fluid flow and acid-base disturbances perturb K+ excretion by the kidneys. In K+-depleted states, K+ secretion is inhibited and the distal tubule and collecting duct reabsorb K+ .
3.
The kidneys, in conjunction with the intestinal tract and bone, play a vital role in regulating plasma [Ca++] and [Pi].
4.